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Published: 3 September 2022

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Hubert, Vaudry, and Laburthe Marc, eds. VIP, PACAP, and related peptides: From gene to therapy. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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NATO Advanced Research Workshop on the Role of Melatonin and Pineal Peptides in Neuroimmunomodulation (1990 Erice, Italy). Role of melatonin and pineal peptides in neuroimmunomodulation. New York: Plenum Press, 1991.

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Bureau de la sécurité des transports du Canada. CN Amérique du Nord train parti à la dérive point milliaire 175, subdivision Grande Cache Latornell (Alberta) 18 janvier 1994. Hull, Qué: Bureau de la sécurité des transports du Canada, 1995.

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Mielczarek, Eugenie V. Iron, nature's universal element: Why people need iron & animals make magnets. New Brunswick, N.J: Rutgers University Press, 2000.

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Chan, W., and Peter White, eds. Fmoc Solid Phase Peptide Synthesis. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199637256.001.0001.

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In the years since the publication of Atherton and Sheppard's volume, the technique of Fmoc solid-phase peptide synthesis has matured considerably and is now the standard approach for the routine production of peptides. The basic problems outstanding at the time of publication of this earlier work have now been, for the most part, solved. As a result, innovators in the field have focussed their efforts to develop methodologies and chemistry for the synthesis of more complex structures. The focus of this new volume is much broader, and covers not only the essential procedures for the production of linear peptides but also more advanced techniques for preparing cyclic, side-chain modified, phospho- and glycopeptides. Many other methods also deserving attention have been included: convergent peptide synthesis; peptide-protein conjugation; chemoselective ligation; and chemoselective purification. The difficult preparation of cysteine and methionine-containing peptides is also covered, as well as methods for overcoming aggregation during peptide chain assembly and a survey of available automated instrumentation.

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Bird, Mark F., and David G. Lambert. Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0026.

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Deorphanization of ORL-1/LC132 in 1995 by reverse pharmacology in two simultaneously published landmark studies added a new member to the opioid family of G-protein coupled receptors. Meunier and Reinscheid used cells expressing recombinant ORL-1 (human) or LC132 (rat) and the presumed intracellular inhibition of cyclic AMP formation to ‘fish’ for endogenous peptide ligands in rat whole-brain and pig hypothalamic extracts. Both studies reported the isolation of a 17-amino-acid peptide, which was named nociceptin and orphanin FQ by the two authors, respectively. The behaviour of the isolated peptide was a complete surprise, as a general hyperalgesia was observed when the peptide was administered at supraspinal sites. We now know that this peptide has, in fact, anti-opioid action, particularly in the medulla. The endogenous peptide exerts a multitude of effects both in the nervous system and, unlike classical opioids, has efficacy in neuropathic pain.

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.

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A new method of distinguishing between organic and inorganic compounds of iron. [S.l: s.n., 1985.

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Peptide Hormones: Effects and Mechanisms of Action (Peptide Hormones). CRC, 1988.

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Tracy, Derek K., and Fiona Gaughran. Treatment with medication: Side effects, adherence, and risk. Edited by Alec Buchanan and Lisa Wootton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198738664.003.0009.

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Antipsychotic medications revolutionized the care of psychosis, but they have brought with them significant side effects and issues around adherence; these latter factors, and informed co-working with patients, are primary drivers for specific medication choices. The data remain limited for polypharmacy and above-maximum dose prescribing, though there may be individuals for whom this is considered. Long-acting injectables (LAIs or ‘depots’) have a good evidence base, and are probably underutilized, though clozapine remains our drug of choice in refractory illness. Forensic-population data show that medications significantly reduce recidivism, including of violent crime. Whilst side effect data are disheartening for both patient and clinician, there are rational management strategies for them all. Novel future therapies being evaluated include acetylcholinergic and glutamatergic enhancers, anti-inflammatory drugs, and the neural peptide oxytocin, to improve negative and cognitive functioning; neuromodulation through rTMS and tDCS are also showing early promise.

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(Editor), Franco Fraschini, and Russel J. Reiter (Editor), eds. Role of Melatonin and Pineal Peptides in Neuroimmunomodulation (Nato Science Series: A:). Springer, 1991.

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Mason, Peggy. Synthesis, Packaging, and Termination of Neurotransmitters. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0012.

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The synthesis, packaging, and termination of action of neurotransmitters are detailed. There are far more varieties of peptide neurotransmitters than there are of low-molecular-weight neurotransmitters. Yet low-molecular-weight neurotransmitters are the ubiquitous workhorses of the nervous system. Acetylcholine, the catecholamines norepinephrine and dopamine, serotonin, glutamate, and GABA are examined in some depth. The vesicular transporters that carry low-molecular-weight neurotransmitters from the cytoplasm into synaptic vesicles are covered. The role of monoamines in affect and mood and the psychotropic effects of monoaminergic drugs are discussed. Principles of catecholamine synthesis are applied to understand phenylketonuria. Uptake of monoamines into neurons is discussed in the context of amphetamine, cocaine, and other drugs of abuse. Stiff-person syndrome, which results from an impairment of GABA synthesis, is introduced. The modes of action for peptide and gaseous neurotransmitters are briefly covered.

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Dickenson, Tony. Endogenous opioids in the CNS. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0019.

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This short and concise paper was the first to unequivocally reveal that there were endogenous opioids in the central nervous system (CNS), identify their peptide nature and sequence, and show that they exerted physiological inhibitory effects. The idea that there were natural opioids fitted with concurrent reports of opiate-binding sites, and this led to the description of multiple receptors with their own families of peptide transmitters. No truly novel opioid drugs have emerged since, and attempts to protect and manipulate the enkephalins for pain control have yet to be successful. This does not detract from this key study, which made us think about pain modulation in a different way, and subsequent work has clearly shown how endogenous opioid signalling is critical in CNS function, perhaps most importantly in endogenous pain control, such as that harnessed by placebo analgesia.

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Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.

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Schulkin, Jay. Social Contact, Gonadal Steroids, and CRF. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198793694.003.0006.

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Chapter 6 begins with a brief discussion of CRF in approach/avoidance behaviors across pre- and postnatal events. What will follow is the description of diverse steroids, in particular gonadal steroids (e.g., testosterone and estrogen) and their effect on CRF and other peptides expression, and finally, sex differences in the expression of CRF in the brain. Importantly, the rapid-fire expression of CRF would serve essential for differing social/ecological demands: parenting is one; responding to conspecifics is another. What evolved is a CRF signature ready for action, responding to changing demands of importance, part of the neural armor in foraging for coherence.

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Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.

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Carter, C. Sue, Inbal Ben-Ami Bartal, and Eric C. Porges. The Roots of Compassion. Edited by Emma M. Seppälä, Emiliana Simon-Thomas, Stephanie L. Brown, Monica C. Worline, C. Daryl Cameron, and James R. Doty. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190464684.013.14.

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Compassion for others and social support have survival value and health benefits. Although compassion is sometimes considered uniquely human, critical components of compassion have been described in nonhuman mammals. Studies originally conducted in social mammals and now in humans have implicated neuropeptide hormones, especially oxytocin, in social cognition, a sense of safety, and the capacity of sociality to permit compassionate responses. In contrast, the related peptide vasopressin and its receptor may be necessary for forming selective relationships and for the apparently paradoxical effects of oxytocin, which can include increases in fear and avoidance. Oxytocin and vasopressin may contribute to sex differences in compassion. Furthermore, among the processes through which oxytocin and vasopressin influence behavior and health are complex effects on the autonomic nervous system. Knowledge of the mechanisms underlying the benefits of compassion offers new insights into the healing power of positive social behaviors and social support.

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Sommer, Claudia. Endogenous opioids mediate stress-induced analgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0031.

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This chapter reviews the landmark paper published in 1990 by Stein et al. and entitled ‘Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation’. Opioids, besides acting centrally as analgesics, may act peripherally upon opioid receptors located on axons and on immune cells. In the publication by Stein et al., it was shown for the first time that endogenous opioid peptides released from immune cells mediate stress-induced analgesia, potentially through opioid receptors on peripheral nerve endings. This finding has led to numerous follow-up studies on endogenous analgesia, including work showing that cannabinoid analgesia is mediated via the peripheral release of opioids, and to the concept of topical opioid analgesia, which may be a good way of using the potent analgesia that opioids can convey, without their CNS-associated side effects.

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McGrayne, Sharon Bertsch, and Eugenie Vorburger Mielczarek. Iron, Nature's Universal Element: Why People Need Iron & Animals Make Magnets. Rutgers University Press, 2000.

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